Evidence map›Paper›PMID 31202118›Full record

ArticleThe Journal of nutritional biochemistry2019

Cyp2b-null male mice are susceptible to diet-induced obesity and perturbations in lipid homeostasis.

Melissa M Heintz, Ramiya Kumar, Meredith M Rutledge, William S Baldwin

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Melissa M HeintzEnvironmental Toxicology Program, Clemson University, Clemson, SC 29634.
Ramiya KumarBiological Sciences, Clemson University, Clemson, SC 29634.
Meredith M RutledgeEnvironmental Toxicology Program, Clemson University, Clemson, SC 29634.
William S BaldwinEnvironmental Toxicology Program, Clemson University, Clemson, SC 29634; Biological Sciences, Clemson University, Clemson, SC 29634. Electronic address: Baldwin@clemson.edu.
Clemson University · US

Funding

The role of acetate fermentation in Entamoeba histolytica growth and infectionP20GM109094 · NIGMS · CLEMSON UNIVERSITY · PI MORRIS, MEREDITH T · 2016 to 2020
$10.4M
The Role of Cyp2b in Toxicant Metabolism and SensitivityR15ES017321 · NIEHS · CLEMSON UNIVERSITY · PI BALDWIN, WILLIAM S · 2009 to 2020
$1.3M
NIEHS NIH HHS R15 ES017321NIGMS NIH HHS P20 GM109094
6 · The paper itself

Abstract

Obesity is an endemic problem in the United States and elsewhere, and data indicate that in addition to overconsumption, exposure to specific chemicals enhances obesity. CYP2B metabolizes multiple endo- and xenobiotics, and recent data suggests that repression of Cyp2b activity increases dyslipidemia and age-onset obesity, especially in males. To investigate the role played by Cyp2b in lipid homeostasis and obesity, we treated wildtype and Cyp2b-null mice with a normal (ND) or 60% high-fat diet (HFD) for 10 weeks and determined metabolic and molecular changes. Male HFD-fed Cyp2b-null mice weigh 15% more than HFD-fed wildtype mice, primarily due to an increase in white adipose tissue (WAT); however, Cyp2b-null female mice did not demonstrate greater body mass or WAT. Serum parameters indicate increased ketosis, leptin and cholesterol in HFD-fed Cyp2b-null male mice compared to HFD-fed wildtype mice. Liver triglycerides and liver:serum triglyceride ratios were higher than their similarly treated wildtype counterparts in Cyp2b-null male mice, indicating a role for Cyp2b in fatty acid metabolism regardless of diet. Furthermore, RNAseq demonstrates that hepatic gene expression in ND-fed Cyp2b-null male mice is similar to HFD-fed WT male mice, suggestive of fatty liver disease progression and a role for Cyp2b in lipid homeostasis. Females did not show as demonstrative changes in liver health, and significantly fewer changes in gene expression, as well as gene expression associated with liver disease. Overall our data indicates that the repression or inhibition of CYP2B may exacerbate metabolic disorders and cause obesity by perturbing fatty acid metabolism, especially in males.

Indexed as

Lipid MetabolismAdipose Tissue, WhiteAnimalsAryl Hydrocarbon HydroxylasesBase SequenceBody WeightCluster AnalysisCytochrome P450 Family 2Diet, High-FatFatty AcidsFemaleGlucose Tolerance TestHomeostasisMaleMiceMice, Inbred C57BLAryl Hydrocarbon HydroxylasesCyp2b9 protein, mouseCytochrome P450 Family 2Fatty AcidsSteroid HydroxylasesTriglyceridesCyp2bNon-alcoholic fatty liver disease (NAFLD)ObesityP450RNAseqTriglycerides

Identifiers

PMID31202118
PMCPMC6642837
OpenAlexW2945189627

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.